LncRNA HOTTIP promotes papillary thyroid carcinoma cell proliferation, invasion and migration by regulating miR-637

Yuan, Qingling; Liu, Yang; Fan, Yuxia; Liu, Zheng; Wang, Xiaoming; Meng, Jia; Geng, Zushi; Zhang, Jing; Lu, Xiaoyan

doi:10.1016/j.biocel.2018.02.013

Cited by 65 publications

(51 citation statements)

References 22 publications

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“…It functions as a tumor suppressor via targeting and downregulating NUPR1 expression, which was shown to lead to the inhibition of proliferation, migration, and invasion in colorectal cancer cells (34). Moreover, supporting our previous results, miR-637 was found to target Akt1 and hamper tumorigenesis in both thyroid carcinoma and pancreatic ductal adenocarcinoma (35,36). MiR-637 could also inhibit Akt phosphorylation and promote melanoma progression (37).…”

Section: Discussionsupporting

confidence: 78%

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

Zeng

Que

Lin

et al. 2020

Preprint

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Background Glioma is the most common primary tumor of the central nervous system. We previously confirmed that zinc finger E-box binding homeobox (ZEB) 2 promotes the malignant progression of glioma, while microRNA-637 (miR-637) is associated with favorable prognosis in glioma. This study investigated the potential interaction between ZEB2 and miR-637 and its downstream signaling pathway in glioma. Methods Chromatin immunoprecipitation, luciferase reporter, and electrophoretic mobility shift assays were used to confirm ZEB2 binding to miR-637. Microarray and bioinformatic analyses were used to investigate targets of miR-637. MTT and EdU assays, transwell assays, and Boyden assays were utilized to assess cell viability, migration, and invasion, respectively. A subcutaneous xenograft model was utilized for analyzing the role of miR-637/high mobility group A1 (HMGA1) interaction in vivo. Immunohistochemistry staining of clinical samples and bioinformatic analysis of the Chinese Glioma Genome Atlas and The Cancer Genome Atlas databases were performed to further confirm the ZEB2/miR-637/HMGA1/vimentin axis. Results ZEB2 was bound directly bind to the E-box elements in the miR-637 promoter and promoted cell proliferation, migration, and invasion via miR-637 downregulation. Subsequent screening confirmed that HMGA1 was a direct target of miR-637, while miR-637 could propagate the malignant phenotype of glioma by suppressing HMGA1 both in vitro and in vivo. Furthermore, the interaction between cytoplasmic HMGA1 and vimentin was observed, and vimentin inhibition could abolish increased migration and invasion induced by HMGA1 overexpression. Notably, the ZEB2/miR-637/HMGA1/vimentin axis was also evident in glioma tissue samples and public glioma datasets, while both HMGA1 and vimentin were associated with an unfavorable prognosis in glioma. Additionally, upregulated HMGA1 and vimentin were found in isocitrate dehydrogenase (IDH) wild-type and 1p/19q non-codeletion diffusely infiltrating glioma. Conclusions We identified an oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin that promotes both migration and invasion in glioma. This not only extends the current understanding of miR-637 regulation in glioma, but also unravels a novel signaling pathway that integrates a transcriptional factor, microRNA, and a chromatin remodeling factor to modulate the malignant phenotype of glioma.

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Section: Discussionsupporting

confidence: 78%

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

Zeng

Que

Lin

et al. 2020

Preprint

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“…Several lncRNAs have been reported to be involved in PTC tumorigenesis and progression. Yuan et al identified a lncRNA, HOTTIP, that is upregulated in human PTC tissues and associated with growth arrest [17]. Zhu et al described the oncogenetic role of lncRNA HOTAIR in PTC and the association between its single nucleotide polymorphisms (SNPs) and PTC risk [18].…”

Section: Discussionmentioning

confidence: 99%

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Duan¹,

Wang²,

Xu³

et al. 2020

J. Cancer

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The incidence of papillary thyroid carcinoma (PTC) has been increased rapidly in recent decades. Long noncoding RNAs (lncRNA) are a class of non-protein-coding transcripts and play critical roles in regulating gene expression and influence biological behaviors of multiple cancers, including PTC. Here, we discovered that lncRNA SNHG3 was significantly downregulated in PTC tissues and cell lines, the expression of SNHG3 was negatively correlated with the TNM stage and poor prognosis of PTC patients. Functional studies illustrated that the depletion of SNHG3 via CRISPR/Cas9 technology promoted the proliferation, migration and invasion abilities of PTC cells. Tumor xenograft models confirmed the tumor-promoting role of silenced SNHG3 in vivo. Further mechanistic analyses revealed that knockout of SNHG3 activated the AKT/mTOR/ERK pathway in PTC cell lines and the mTOR inhibitor AZD8055 abrogated the tumor-promoting effect induced by SNHG3 inhibition. Taken together, our findings identified a lncRNA SNHG3 that functions its tumor-suppressor role during PTC development and SNHG3 might serve as a promising candidate for target therapy of PTC.

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“…Increasing evidence indicates that HOTTIP is overexpressed in prostate cancer, lung cancer, and pancreatic cancer . HOTTIP knockdown impedes cell viability, proliferation, invasion, and angiogenesis in human cancer cells, therefore it is been identified as an oncogenic long noncoding RNA (lncRNA). In addition, HOTTIP overexpression is in association with poor prognosis in cancers .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

Zheng

Mao

Dong

et al. 2018

J Cellular Molecular Medi

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HOXA transcript at the distal tip (HOTTIP) has been shown to be up‐regulated in a variety of cancers and is identified as an oncogenic long noncoding RNA. However, the biological role of HOTTIP in liver fibrosis is unclear. Here, we reported that HOTTIP was specifically overexpressed in activated hepatic stellate cells (HSCs). HOTTIP knockdown suppressed the activation and proliferation of HSCs. Luciferase reporter assay showed that HOTTIP and serum response factor (SRF) were targets of miR‐150. RNA binding protein immunoprecipitation assay indicated the interaction between miR‐150 and HOTTIP. Further study revealed that HOTTIP increased SRF expression as a competing endogenous RNA for miR‐150, thus prompting HSC activation. Taken together, we provide a novel HOTTIP‐miR‐150‐SRF signalling cascade in liver fibrosis.

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LncRNA HOTTIP promotes papillary thyroid carcinoma cell proliferation, invasion and migration by regulating miR-637

Cited by 65 publications

References 22 publications

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

Oncogenic ZEB2/miR-637/HMGA1 signaling axis targeting vimentin promotes the malignant phenotype of glioma

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Long noncoding RNA HOTTIP mediates SRF expression through sponging miR‐150 in hepatic stellate cells

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